Maternal depressive symptoms and young people's higher education participation and choice of university: Evidence from a longitudinal cohort study.

BACKGROUND: Participation in higher education has significant and long-lasting consequences for people's socioeconomic trajectories. Maternal depression is linked to poorer educational achievement for children in school, but its impact on university attendance is unclear. METHODS: In an English longitudinal cohort study (N = 8952), we explore whether young people whose mothers experienced elevated depressive symptoms are less likely to attend university, and the role of potential mediators in the young person: educational achievement in school, depressive symptoms, and locus of control. We also examine whether maternal depressive symptoms influence young people's choice of university, and non-attendees' reasons for not participating in higher education. RESULTS: Young people whose mothers experienced more recurrent depressive symptoms were less likely to attend university (OR = 0.88, CI = 0.82,0.94, p < 0.001) per occasion of elevated maternal depressive symptoms) after adjusting for confounders. Mediation analysis indicated this was largely explained by educational achievement in school (e.g., 82.7 % mediated by age 16 achievement) and locus of control at 16. There was mixed evidence for an impact on choice of university. For participants who did not study at university, maternal depressive symptoms were linked to stating as a reason having had other priorities to do with family or children (OR: 1.17, CI = 1.02,1.35). LIMITATIONS: Lack of data on the other parent's depression, loss to follow-up, possibly selective non-response. CONCLUSIONS: Young people whose mothers experience elevated depressive symptoms on multiple occasions are less likely to participate in higher education; educational achievement in secondary school, but not the young people's own depressive symptoms, substantially mediated the effect.

The causal effects of education on adult health, mortality and income: evidence from Mendelian randomization and the raising of the school leaving age.

BACKGROUND: On average, educated people are healthier, wealthier and have higher life expectancy than those with less education. Numerous studies have attempted to determine whether education causes differences in later health outcomes or whether another factor ultimately causes differences in education and subsequent outcomes. Previous studies have used a range of natural experiments to provide causal evidence. Here we compare two natural experiments: a policy reform, raising the school leaving age in the UK in 1972; and Mendelian randomization. METHODS: We used data from 334 974 participants of the UK Biobank, sampled between 2006 and 2010. We estimated the effect of an additional year of education on 25 outcomes, including mortality, measures of morbidity and health, ageing and income, using multivariable adjustment, the policy reform and Mendelian randomization. We used a range of sensitivity analyses and specification tests to assess the plausibility of each method's assumptions. RESULTS: The three different estimates of the effects of educational attainment were largely consistent in direction for diabetes, stroke and heart attack, mortality, smoking, income, grip strength, height, body mass index (BMI), intelligence, alcohol consumption and sedentary behaviour. However, there was evidence that education reduced rates of moderate exercise and increased alcohol consumption. Our sensitivity analyses suggest that confounding by genotypic or phenotypic confounders or specific forms of pleiotropy are unlikely to explain our results. CONCLUSIONS: Previous studies have suggested that the differences in outcomes associated with education may be due to confounding. However, the two independent sources of exogenous variation we exploit largely imply consistent causal effects of education on outcomes later in life.

Common health conditions in childhood and adolescence, school absence, and educational attainment: Mendelian randomization study.

Good health is positively related to children's educational outcomes, but relationships may not be causal. Demonstrating a causal influence would strongly support childhood and adolescent health as important for education policy. We applied genetic causal inference methods to assess the causal relationship of common health conditions at age 10 (primary/elementary school) and 13 (mid-secondary/mid-high school) with educational attainment at 16 and school absence at 14-16. Participants were 6113 children from the Avon Longitudinal Study of Parents and Children (ALSPAC). Exposures were symptoms of attention-deficit hyperactivity disorder (ADHD), autism spectrum disorder (ASD), depression, asthma, migraines and BMI. Genetic liability for these conditions and BMI was indexed by polygenic scores. In non-genetic, multivariate-adjusted models, all health conditions except asthma and migraines were associated with poorer attainment and greater school absence. School absence substantially mediated effects of BMI (39.9% for BMI at 13) and migraines (72.0% at 10), on attainment with more modest mediation for emotional and neurodevelopmental conditions. In genetic models, a unit increase in standardized BMI at 10 predicted a 0.19 S.D. decrease (95% CI: 0.11, 0.28) in attainment at 16, equivalent to around a 1/3 grade lower in all subjects, and 8.7% more school absence (95% CI:1.8%,16.1%). Associations were similar at 13. Genetic liability for ADHD predicted lower attainment but not more absence. Triangulation across multiple approaches supports a causal, negative influence on educational outcomes of BMI and ADHD, but not of ASD, depression, asthma or migraine. Higher BMI in childhood and adolescence may causally impair educational outcomes.

The causal effects of health conditions and risk factors on social and socioeconomic outcomes: Mendelian randomization in UK Biobank.

BACKGROUND: We aimed to estimate the causal effect of health conditions and risk factors on social and socioeconomic outcomes in UK Biobank. Evidence on socioeconomic impacts is important to understand because it can help governments, policy makers and decision makers allocate resources efficiently and effectively. METHODS: We used Mendelian randomization to estimate the causal effects of eight health conditions (asthma, breast cancer, coronary heart disease, depression, eczema, migraine, osteoarthritis, type 2 diabetes) and five health risk factors [alcohol intake, body mass index (BMI), cholesterol, systolic blood pressure, smoking] on 19 social and socioeconomic outcomes in 336 997 men and women of White British ancestry in UK Biobank, aged between 39 and 72 years. Outcomes included annual household income, employment, deprivation [measured by the Townsend deprivation index (TDI)], degree-level education, happiness, loneliness and 13 other social and socioeconomic outcomes. RESULTS: Results suggested that BMI, smoking and alcohol intake affect many socioeconomic outcomes. For example, smoking was estimated to reduce household income [mean difference = -£22 838, 95% confidence interval (CI): -£31 354 to -£14 321] and the chance of owning accommodation [absolute percentage change (APC) = -20.8%, 95% CI: -28.2% to -13.4%], of being satisfied with health (APC = -35.4%, 95% CI: -51.2% to -19.5%) and of obtaining a university degree (APC = -65.9%, 95% CI: -81.4% to -50.4%), while also increasing deprivation (mean difference in TDI = 1.73, 95% CI: 1.02 to 2.44, approximately 216% of a decile of TDI). There was evidence that asthma decreased household income, the chance of obtaining a university degree and the chance of cohabiting, and migraine reduced the chance of having a weekly leisure or social activity, especially in men. For other associations, estimates were null. CONCLUSIONS: Higher BMI, alcohol intake and smoking were all estimated to adversely affect multiple social and socioeconomic outcomes. Effects were not detected between health conditions and socioeconomic outcomes using Mendelian randomization, with the exceptions of depression, asthma and migraines. This may reflect true null associations, selection bias given the relative health and age of participants in UK Biobank, and/or lack of power to detect effects.

EARLY, LATE OR NEVER? WHEN DOES PARENTAL EDUCATION IMPACT CHILD OUTCOMES?

We estimate the causal effect of parents' education on their children's education and examine the timing of the impact. We identify the causal effect by exploiting the exogenous shift in (parents') education levels induced by the 1972 minimum school leaving age reform in England. Increasing parental education has a positive causal effect on children's outcomes that is evident in preschool assessments at age 4 and continues to be visible up to and including high-stakes examinations taken at age 16. Children of parents affected by the reform attain results around 0.1 standard deviations higher than those whose parents were not impacted.